BackgroundWe investigated whether microRNA-206 (miR-206) is abnormally expressed in patients with coronary artery disease (CAD). The potential mechanism by which miR-206 may regulate CAD progression was also studied.Material/MethodsA total of 78 CAD patients in the case group and 65 subjects in the control group were enrolled in this study so that the correlation between miR-206 and CAD could be accurately determined. Serum total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides were detected using a biochemistry analyzer. MiR-206 and vascular endothelial growth factor (VEGF) expression levels were tested using either reverse transcription polymerase chain reaction or western blot. Associations between miR-206 expression and different clinicopathological features of CAD patients were also analyzed. CAD cells were transfected with miR-206 mimic (miR-206), its negative control (miR-NC), miR-206 inhibitor (anti-miR-206), and its negative control (anti-miR-NC), respectively. Flow cytometry was conducted to explore the function of miR-206 in CAD cell apoptosis after transfection. Moreover, transwell assay was carried out to study the migratory ability of endothelial progenitor cells (EPCs) in CAD patients.ResultsMiR-206 expression was enriched in both diseased EPCs and plasma of CAD patients. No significant correlation was found between decrease in miR-206 expression and different clinicopathological features. In addition, miR-206 significantly suppressed the viability and invasion of EPCs in CAD patients, and it promoted the apoptosis of their EPCs. Moreover, we found that miR-206 is able to inhibit VEGF expression.ConclusionsAs suggested by our study, MiR-206 can be a novel benign biomarker for CAD because it may regulate VEGF expression.
Background and aim Secreted frizzled-related protein 2 (sFRP2) has been reported to be involved in cardiovascular diseases. However, its role in cardiac hypertrophy induced by pressure overload is still elusive. We aimed to examine the role of sFRP2 in the development of cardiac hypertrophy in vivo and in vitro. Methods and results Following cardiac hypertrophy stimulated by aortic banding (AB), the expression of sFRP2 was downregulated in the hypertrophic ventricle. Adeno-associated virus 9 (AAV9) was injected through the tail vein to overexpress sFRP2 in the mouse myocardium. Overexpression of sFRP2 alleviated cardiomyocyte hypertrophy and interstitial fibrosis, as identified by the reduced cardiomyocyte cross-sectional area, heart weight/body weight ratio, and left ventricular (LV) collagen ratio. Additionally, sFRP2 decreased cardiomyocyte apoptosis induced by pressure overload. Western blot showed that sFRP2 prevented the expression of active β-catenin. The Wnt/β-catenin agonist LiCl (1 mmol/kg) abolished the inhibitory effects of sFRP2 on cardiac hypertrophy and apoptosis, as evidenced by the increased cross-sectional area and LV collagen ratio and the deterioration of echocardiographic data. Conclusion Our study indicated that decreased sFRP2 levels were observed in failing mouse hearts. Overexpression of sFRP2 attenuated myocyte hypertrophy and interstitial fibrosis induced by hypertrophic stimuli by inhibiting the Wnt/βcatenin pathway. We revealed that sFRP2 may be a promising therapeutic target for the development of cardiac remodeling.
The most frequent tachyarrhythmia in the world is atrial fibrillation (AF). The global prevalence of AF is currently 37,574 million (0.51% of the global population), by 2050, the morbidity of AF is expected to rise by more than 60% (Chugh et al., 2014;Lippi et al., 2021). It has a high mortality, morbidity, hospitalization rates and economic spending, all of which put a strain on the global health system and make it a global health threat (Hindricks et al., 2021). The number of AF patients in China is estimated to be around 4,870,000 (Wang et al., 2018). The most effective treatment for AF, radiofrequency catheter ablation (RFCA), is strongly recommended in the 2020 ESC guidelines, greatly lowering the burden of symptoms (Kalla et al., 2017). Patients' symptoms (palpitation, fatigue, recurrence, etc.) cannot be eased immediately after RFCA, putting their psychological well-being at risk. The psychological problem is more evident in the postoperative "Blanking Period" (Sang et al., 2013).The first 3 months after surgery is known as the "Blanking Period,"
Background: This study aimed to identify the microRNAs implicated in atrial fibrillation (AF) to investigate the molecular mechanisms underlying the role of microRNAs in ablation-based AF treatment. Methods: Real-time polymerase chain reaction (PCR) and microRNA microarrays were utilized to measure the profiles of microRNA expression in AF to identify differentially expressed microRNAs. Enzyme-linked immunosorbent assay, real-time PCR, Western blot analysis, and immunohistochemistry assays were also performed to investigate the regulatory relationships among various factors implicated in AF. Finally, bioinformatic tools and luciferase assays were used to confirm the roles of miR-155-5p, miR-24-3p, endothelial nitric oxide synthase (eNOS), and nitric oxide (NO) in the pathogenesis of AF.Results: We demonstrated that the levels of miR-155-5p and miR-24-3p were greatly reduced in postablation AF patients compared with those AF patients not treated by ablation. Furthermore, the NO level in the AF+ group was much lower than that of the AF− group. Finally, in a swine model of AF, evident upregulation of miR-155-5p and miR-24-3p was found in AF pigs, whereas the ablation treatment reduced the levels of miR-155-5p and miR-24-3p in AF pigs.On contrary, as targets of miR-155-5p and miR-24-3p, the levels of eNOS and NO increased when the expression of miR-155-5p and miR-24-3p decreased.Conclusion: MiR-155-5p and miR-24-3p are involved in the pathogenesis of AF via regulating the expression of eNOS and the production of NO. In addition, ablation treatment helps the recovery from AF by reducing the expression of miR-155-5p and miR-24-3p. K E Y W O R D S ablation, atrial fibrillation, endothelial nitric oxide synthase, expression profiling, microarray, microRNA, nitric oxide 1 | INTRODUCTION As one of the most frequently diagnosed chronic arrhythmia, atrial fibrillation (AF) significantly affects the quality of life of its patients. Triggered by an irregular ventricular rate and the disorder in atrial contraction, AF is featured by a high rate (up to 600 beats/min) of asynchronous depolarization of atrial cells. 1 The prevalence of AF is about 2% in developed countries and the mean age of AF patients is about 80 years old. 2 Although J Cell Biochem. 2019;120:4451-4462.wileyonlinelibrary.com/journal/jcb
Background: Amiodarone is an antiarrhythmic drug that is frequently used to control atrial fibrillation (AF). Many patients with AF are afraid of the risk of ablation and take amiodarone, some patients develop amiodarone-induced thyrotoxicosis (AIT AF (35% vs. 3.33%; p = 0.01) were higher, while those for atrial flutter (15% vs. 3.33%; p = 0.17) and atrial tachycardia (15% vs. 6.67%; p = 0.31) were similar, as was the recovery of conduction of pulmonary vein potential (15% vs. 30%; p = 0.191). In AIT vs. control group, atrial tachyarrhythmia recurrence rate was higher at 3 months (45% vs. 16.67%, p = 0.032) (Cardiol J 2016; 23, 4: 416-421)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.